Coagulopathy in traumatic brain injury

Alexiou, George Α.; Pahatouridis, Dimitrios; Voulgaris, Spyridon

doi:10.1016/j.injury.2010.06.019

Cited by 137 publications

(6 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hemocoagulation disorder is a common and important consequence of TBI, with a reported incidence from 15 to 100% [1]. A number of literatures demonstrate that posttraumatic coagulopathy appears to be linked to secondary cerebral insults and often results in a poor clinical prognosis [8–11].…”

Section: Discussionmentioning

confidence: 99%

“…We also found that coagulation derangement was strongly associated with early PTCI. It has been hypothesized that the thrombotic-fibrinolytic imbalance after moderate or severe TBI may provoke an ischemic diathesis by the activation of hemostatic mechanisms and the inhibition of natural anticoagulation cascades [1, 2, 21, 22]. After head trauma, the release and upregulation of thromboplastin from the damaged parenchymal brain cells sequentially activate the procoagulant proteins of the extrinsic clotting pathway, which is represented by PT values.…”

Section: Discussionmentioning

confidence: 99%

“…The diagnosis was made on MRI by visualization of a well-demarcated region, in an arterial vascular distribution, of low signal on T1-weighted images, high signal on conventional T2-weighted or fluid attenuation inversion recovery sequences, and of high signal on diffusion weighted images, indicating diminished perfusion, associated with a corresponding decrease in signal on the apparent diffusion coefficient map [1]. …”

Section: Clinical Materials and Methodsmentioning

confidence: 99%

“…Patients were evaluated and treated following the currently accepted international guidelines [1]. All patients were offered clinical and radiological evaluation at 3 months after injury via outpatient interviews and CT images of the brain.…”

Section: Clinical Materials and Methodsmentioning

confidence: 99%

“…The incidence is reported to vary between 15% and 100% [1]. It begins with the massive release of thrombin or tissue factor (TF), from damaged brain cells, following the activation of hemostatic mechanisms/coagulation pathway.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

The Influence of Hemocoagulation Disorders on the Development of Posttraumatic Cerebral Infarction and Outcome in Patients with Moderate or Severe Head Trauma

Chen¹,

Xue²,

Guo³

et al. 2013

BioMed Research International

View full text Add to dashboard Cite

Posttraumatic cerebral infarction (PTCI) is a severe secondary insult of head injury and often leads to a poor prognosis. Hemocoagulation disorder is recognized to have important effects on hemorrhagic or ischemic damages. We sought to assess if posttraumatic hemocoagulation disorders were associated with cerebral infarction, and evaluate their influence on outcome among patients with moderate or severe head trauma. In this study, PTCI was observed in 28 (10.57%) of the 265 patients within the first week after injury. In multivariate analysis, the thrombocytopenia (odds ratio (OR) 2.210, 95% confidence interval (CI) 1.065–4.674), abnormal prothrombin time (PT) (OR 3.241, 95% CI 1.090–7.648), D-dimer (>2 mg/L) (OR 7.260, 95% CI 1.822–28.076), or disseminated intravascular coagulation (DIC) scores (≥5) (OR 4.717, 95% CI 1.778–12.517) were each independently associated with an increased risk of PTCI. Admission Glasgow Coma Scale (GCS) score, abnormal activated partial thromboplastin time (APTT) and fibrinogen, and D-dimer (>2 mg/L) and DIC scores (≥5) showed an independent predictive effect on poor outcome. In conclusion, recognition of this important treatable cause of PTCI and the associated risk factors may help identify the group at risk and tailor management of patients with TBI.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Clinical Materials and Methodsmentioning

confidence: 99%

Section: Clinical Materials and Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The Influence of Hemocoagulation Disorders on the Development of Posttraumatic Cerebral Infarction and Outcome in Patients with Moderate or Severe Head Trauma

Chen¹,

Xue²,

Guo³

et al. 2013

BioMed Research International

View full text Add to dashboard Cite

show abstract

Platelet‐like particles reduce coagulopathy‐related and neuroinflammatory pathologies post‐experimental traumatic brain injury

et al. 2021

View full text Add to dashboard Cite

Coagulopathy may occur following traumatic brain injury (TBI), thereby negatively affecting patient outcomes. Here, we investigate the use of platelet‐like particles (PLPs), poly(N‐isopropylacrylamide‐co‐acrylic‐acid) microgels conjugated with a fibrin‐specific antibody, to improve hemostasis post‐TBI. The objective of this study was to diminish coagulopathy in a mouse TBI model (controlled cortical impact) via PLP treatment, and subsequently decrease blood–brain barrier (BBB) permeability and neuroinflammation. Following an acute intravenous injection of PLPs post‐TBI, we analyzed BBB permeability, ex vivo coagulation parameters, and neuroinflammation at 24 hr and 7 days post‐TBI. Both PLP‐treatment and control particle‐treatment had significantly decreased BBB permeability and improved clot structure 24 hr post‐injury. Additionally, no significant change in tissue sparing was observed between 24 hr and 7 days for PLP‐treated cohorts compared to that observed in untreated cohorts. Only PLP‐treatment resulted in significant reduction of astrocyte expression at 7 days and percent difference from 24 hr to 7 days. Finally, PLP‐treatment significantly reduced the percent difference from 24 hr to 7 days in microglia/macrophage density compared to the untreated control. These results suggest that PLP‐treatment addressed acute hypocoagulation and decreased BBB permeability followed by decreased neuroinflammation and fold‐change tissue loss by 7 days post‐injury. These promising results indicate that PLPs could be a potential therapeutic modality for TBI.

show abstract

Tissue factor release following traumatic brain injury drives thrombin generation

Hubbard

Sim

Saatman

et al. 2022

Research and Practice in Thrombosis and Haemostasis

View full text Add to dashboard Cite

Background Traumatic brain injury (TBI) results in neurovascular damage that initiates intrinsic mechanisms of hypercoagulation, which can contribute to the development of life‐threatening complications, such as coagulopathy and delayed thrombosis. Clinical studies have hypothesized that tissue factor (TF) induces hypercoagulability after TBI; however, none have directly shown this relationship. Objectives In the current study, we took a stepwise approach to understand what factors are driving thrombin generation following experimental TBI. Methods We employed the contusion‐producing controlled cortical impact (CCI) model and the diffuse closed head injury (CHI) model to investigate these mechanisms as a function of injury severity and modality. Whole blood was collected at 6 hours and 24 hours after injury, and platelet‐poor plasma was used to measure thrombin generation and extracellular vesicle (EV) TF. Results We found that plasma thrombin generation, dependent on TF present in the plasma, was greater in CCI‐injured animals compared to sham at both 6 hours (120.4 ± 36.9 vs 0.0 ± 0.0 nM*min endogenous thrombin potential) and 24 hours (131.0 ± 34.0 vs 32.1 ± 20.6 nM*min) after injury. This was accompanied by a significant increase in EV TF at 24 hours (328.6 ± 62.1 vs 167.7 ± 20.8 fM) after CCI. Further, EV TF is also increased at 6 hours (126.6 ± 17.1 vs 63.3 ± 14.4 fM) but not 24 hours following CHI. Conclusion TF‐mediated thrombin generation is time‐dependent after injury and TF increases resolve earlier following CHI as compared to CCI. Taken together, these data support a TF‐mediated pathway of thrombin generation after TBI and pinpoint TF as a major player in TBI‐induced coagulopathy.

show abstract

Coagulopathy in traumatic brain injury

Cited by 137 publications

References 4 publications

The Influence of Hemocoagulation Disorders on the Development of Posttraumatic Cerebral Infarction and Outcome in Patients with Moderate or Severe Head Trauma

The Influence of Hemocoagulation Disorders on the Development of Posttraumatic Cerebral Infarction and Outcome in Patients with Moderate or Severe Head Trauma

Platelet‐like particles reduce coagulopathy‐related and neuroinflammatory pathologies post‐experimental traumatic brain injury

Tissue factor release following traumatic brain injury drives thrombin generation

Contact Info

Product

Resources

About